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Anti-infective therapy Flashcards

1
Q

how do bacteria become resistant to antibiotics

A

acquiring mutations that counteracts antibiotics by doing the following:

  • degradation/modification of antibiotic (beta lactamases)
  • reduction in the bacterial antibiotic concentration (interference with entry [lipid coat/loss of porins from which antibiotics enter/ creation of efflux pumps])
  • modification of antibiotic target(alteration in cell wall precursor/ changes in target enzymes[penicillin binding protein]/alteration in ribosomal binding site)
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2
Q

how can the continued selection of highly resistant organisms be prevented

A

administer a high dose (high AUC/MIC ration [area under curve/mean inhibitory concentration) because the more rapid the selective pressure on the bacteria the less likely the selection for a highly resistant traits

short course of antibiotic (<5days )

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3
Q

what are the strategies that underline optimal antibiotic usage

A

administer a high dose (high AUC/MIC ration [area under curve/mean inhibitory concentration)

short course of antibiotic (<5days )

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4
Q

how do bacteria transfer antibiotic traits

A

those bacteria confer antibiotic resistance to others by:
conjugation (plasmid transferred)
transduction (DNA is injected from a phage)
transformation (DNA is donated to another bacteria)

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5
Q

what is the mean inhibitory concentraion

A

the least amount of antibiotic needed to prevent visible growth of a bacterium

the amount administered should be just above the MIC for half of the duration of treatment

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6
Q

steps for antibiotic regimen

A

know if its a bacteria infection (WBC count mainly neutrophils [viral increases lymphocytes] or procalcitonin can differentiate better)
locate the site of infection
take into consideration nosocomial infections/previous antibiotic use
switch to narrow-spectrum antibiotic within 3 days

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7
Q

steps for antibiotic regimen

A

know if its a bacteria infection (WBC count mainly neutrophils [viral increases lymphocytes] or procalcitonin can differentiate better)
locate the site of infection
take into consideration nosocomial infections/previous antibiotic use
take into consideration the patents status (immunity, hepatic function , age, severity of illness)
switch to narrow-spectrum antibiotic within 3 days

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8
Q

when do you switch antibiotics

A

in the case of a new infection/superinfection

superinfection indications
new fever
increased peripheral WBC
increased inflammatory exudate at the site of injection (sign for catheter associated infection)
increased polymorphonuclear lymphocytes on gram stain

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9
Q

name beta lactam antibiotics and their MOA and toxicity

A

penicillin, cephalosporins, carbapenems

MOA: B lactam rings binds to penicillin binding proteins that’s important for bacterial cell wall cross-linking

since they require active division of bacteria they are all antagonized by bacteriostatic antibiotics

all peneillins have short half life

toxicity:
hypersensitivity= anaphylaxis
nephrotoxicity (aminoglycosides with cephalosporins)
increased prothrombin time (cephalosporines interfere with Vit K)
encephalopathy in the elderly (cefepime)
ceftriaxone is secreted in the blie and can cause cholecystitis
seizures in patients with renal dysfunction

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10
Q

indications for penicillins and their dosing

A

S. pyogenes
S. viridans
Neiserria menengiditis
s. pneumoniae

IM/IV with a short half life, excreted by the kidneys, narrow spectrum

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11
Q

what’s the difference between aminopenicillins and penicillin’s

A

aminopenicillins are modified penicillins that can survive stomach acidity thus can be given orally

ampicillin plus aminoglycoside is treatment of choice for enterococci
amoxicillin-clavulanate are for H. influenzae staphylococcus

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12
Q

what are penicillinase resistant penicilins and their indication

A

Nafcillin and oxacillin

modified so it is resistant to penicillinase produced by penicillin resistant strains

it has hepatic clearance so dose doesn’t have to be adjusted in renal dysfunction

primarily used for methicillin sensitive staph aureus and cellulitis

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13
Q

name the usage of different types of cephalosporines (different generations)

A

ALL generations inhibit cell wall synthesis/bactericidal

1st gen: G positive cocci, for surgical prophylaxes, Cant cross BBB
2nd gen: aerobic/anaerobic G negative bacilli, vit k deficiency, (decreases prothrombin time )
3rd gen: G negative bacilli H. influenza/N. gonorrhea / N. menegiditis. for community acquired pneumonia and meningitis
4th gen: broad spectrum, pseudomonas and S. aureus and nosocomial infections
5th gen: MSSA/MRSA and penicillin resistant S. pneumoniae. penetrates all tissue (BBB as well). good for community acquired pneumonia

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14
Q

adverse reactions of cephalosporines

A 
hypersensitivity reactions
autoimmune hemolytic anemia
disulfiram like reaction
vit k deficiency
nephrotoxic synergy with aminoglycosides
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15
Q

Cephalosporine mnemonic

A

1st gen: az ale cefAZolin, cefALExin
2nd gen: process of elimination
3rd: 3T’s cefTRIaxone, cefTAXime, cefTAZidime
4th gen:4 cefourpime or Cefepime
5th: cefSTARoline or ceftaroline. star has 5 arms

from a YouTube video, don’t blame me on how bad that is

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16
Q

carbapenems, structure, usages and side effects

A

member of beta lactams
for high risk infections and suspected multi drug resistant bacteria
modified B lactam ring that’s highly resistant to cleavage (resistance to beta lactamase)
it penetrates all tissue
people who are allergic to penicillin might be allergic to carbapenems

used most G positive
G negative include listeria and nocardia
usage for suspected mixed aerobic and anaerobic (sepsis, pyelonephritis, meningitis)and nosocomial infection

Side effects: cause seizures in high doses, dramatically changes normal flora

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17
Q

aminoglycosides MOA

A

have a positive charge that is activated by beta lactamas (thus don’t use with beta lactam antibiotics)
they inhibit protein synthesis

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18
Q

toxicity of aminoglycosides

A

low therapeutic index compared to toxicity
ototoxicity: neomycin has the highest risk of toxicity
nephrotoxicity:
damage to proximal tubes, reversible
significant reduction in GFR
higher incidence in the elderly

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19
Q

dosing of aminoglycosides

A

once a day to reduce (but not eliminate) nephrotoxicity but not recommended for enterococcal endocarditis
good for gram negative bacteria
require active bacterial growth
affect starts after 2 hours

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20
Q

MOA of glycopeptides and name some

A

binds a cell wall precures that’s different to the b lactam antibiotics and messes the permeability
also affects RNA synthesis
require active bacterial growth (don’t use bacteriostatic)
vancomycin is an example

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21
Q

vancomycin toxicity

A

rapid infusion leads to red man syndrome (flushing of the upper body) which is prevented by a 1hour long infusion
phlebitis is common (vein inflammation)
ototoxicity is preceded by tennitus, so stop when tinnitus presents

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22
Q

what do you use vancomycin for

A 
MRSA
penicillin resistant S. pneumoniae 
coagulase negative staphylococci
penicillin allergic S. pyogenes
excellent against enterococcus but vancomycin resistant enterococci are emerging

indications
sepsis Coagulase negative staphylococcal
endocarditis
pneumococcal meningitis S. pneumonia

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23
Q

macrolides and ketolides MOA and side effects

A

same mechanism that inhibits RNA dependent protein synthesis by blocking protein exit from ribosome by binding to 50s
bacteriostatic/ bactericidal

SE:
GI irritation with erythromycin is the major toxicity
hypersensitivity reactions
exacerbations of myasthenia gravis

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24
Q

indications for macrolides

A 
Gram positive 
community acquired pneumonia
legionella pneumophilia
mycoplasma
helicobacter pylori
mycobacterium avium intercellulare!! (clarithromycin )
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25
drugs against MRSA
``` vancomycin (red man syndrome/phlebitis) ceftaroline (5th gen cephalosporin) clarithromycin (macrolide) clindamycin linezolid daptomycin ```
26
clindamycin (NOT A MACROLIDE) MOA and side effects
increased C. diff which releases toxins that causes pseudomembranous colitis which can lead to toxic megacolon MOA: binds 50S and prevents protein synthesis used to treat anaerobic lung abscesses and toxoplasmosis reduce pyogenes toxin pharyngitis in S. pyogenes
27
tetracyclines MOA, Side effects, usages
MOA binds 30s stops protein synthesis (bacteriostatic) side effect: photosensetivity interfers with dental enamel formation in children fatty liver disease worsens azotemia calcium and magnisum lowers its absorption usages: uncomplicated UTI lyme disease, rikketsial infections, chlamydia in combinations with others in inflammatory pelvic disease Burcellosis intraadominal and soft tissue infection
28
chloramphenicol MOA, side effects and usages
has a benzen group. binds 50s of the ribosome and prevents protein synthesis, bacteriostatic to most but bacteriocidal in H.influenza, S. pneumoniae and N. meningiditis SE: idiosyncratic anaplastic anemia because of bone suppression. this also elevates serum iron broad spectrum activity, can be used in a penicillin allergic patient not considered the treatment of choice of anything well absorbed in liver and passes the BBB
29
quinolones MOA, side effects
Inhibits DNA gyrase(important for cloiling) and tropoisomirase (for DNA segregation to daughter cells). rapidly cidal with concentration dependent killing ``` SE: nausea, anorexia allergic reaction (gemifloxacin) arthropathy and tendonitis (thus not recommended in children) gatifloxacin causes hyper/hypo glycemia moxifloxacin prolongs QT interval ```
30
ciprofloxacin usage
quinolone for pseudomonas (same as Cefepime) good for gram negative bacteria kills mycoplasma, chlamydia and ureaplasma recommended for UTI/peritonitis, rethritis, travelers diarrhea, typhoid fever, salmonella, cat scratch disease
31
Levofloxacin, gatifloxacin, moxifloxacin, gemifloxacin usage
good activity agaisnt strep pneumoniae covers MSSA recommended for ommunity aquired pneumonia recommended for skin infections
32
antibiotics that bind 50s
``` macrolides chloramphenicol clindamycin linezolid synercid ```
33
linezolid MOA and usage
binds 50s side effects: thrombocytopenia inhibitor of MAO (avoid tyramine: an amino acid that helps regulate blood pressure, and is increased in quantitiy following MOA inhibition. avoid SSRI) strictly gram positive bacteriostatic for VRE vancomycine resistant enterococci and MRSA
34
synercid MOA and usage
combination of quinupristin and dalfopristin bind 50s SE: myalgias and arthralgias force the discontinuation of the drug used against VRE and MRSA recommended for VRE
35
daptomycin MOA, SE and usage
large cyclic lipopeptide tat binds and depolarizes bacterial membranes rapidly cidal with concentration dependent killing SE: toxicity causes muscle pains, weakness associated with creatine phosphokinase leak(catalyzes the conversion of creatine and uses adenosine triphosphate) (don't coadminister statins) could cause peripheral neuropathy usages: VRE MRSA S. pyogenes approved for complicated skin soft tissue infection and MRSA inactivated by surfactant (shouldn't be used to treat pneumonia)
36
rapidly cidal antibiotics
quinolones prevent DNA replication | daptomycin lipopeptide that depolarize membranes
37
drugs for VRE vancomycin resistant enterococci
daptomycin linezolid synercid
38
metronidazole MOA and SE and usages
electron acceptor produces free radicals that damages bacterial DNA antabus like reaction (wtf is wrong with them, its called Disulfaram-like reaction which causes flushing and GI symptoms) should be avoided in pregnancy excellent against anaerobes, amoebae giardia and trichomonas indicated with other antibiotics for mixed infections treatment of choice for C. diff also a combination for H. pylori
39
sulfonamides MOA, SE and usages
MOA:blocks folic acid synthesis by inhibiting PA acid incorporation, sulfonamides potentiate this by inhibiting dihydroflate reductase SE: steven johnson syndrome (blistering) hemolytic anemia seen in G6PD deficient patients (makes energy in RBC) ``` Usages: broad spectrum for G+ and G- used for uncomplicated UTI treatment of choice for nocardia Trimethoprim-sulfamethoxazole is the drug of choice for pneumocystis prophylaxis and treatment ```
40
drugs that inhibits folic acid synthesis
trimethoprim | sulfonamides
41
drugs for uncomplicated UTI
tetracyclines | sulfonamides
42
treatment of choice for nocardia, C. diff and enterococci, pneumocystis prophylaxis
ampicillin plus aminoglycoside is treatment of choice for enterococci sulfonamides are the treatment of choice for nocardia metronidazole is the treatment of choice for C. diff Trimethoprim-sulfamethoxazole is the drug of choice for pneumocystis prophylaxis and treatment
43
are fungi eukaryotes or prokaryotes
Eukaryotes, their cells have nucleii
44
Amphotericin B: MOA, SE, usages
MOA: form rod-like structures that bind to ergosterol in the fungal membrane that creates pores which causes potassium to leak out. its rapidly cidal SE: Nephrotoxicity (reduced by hydration using normal saline, but permanent damage with prolonged therapy) Fever in all preparation (slow administration reduces the severity) phlebitis (requiring administration by central intravenous line since its larger, it reduces the inflammation) treatment of choice for systemic fungal infections effective against most except those (candida Lusitania, fusarium, pseudalleschieria boydii) very high cost
45
azoles: MOA, SE, usages, DDI with amphotericin B
inhibit cytochrome p450 demethylation which results in decreased ergosterol production and altered fungal membrane permeability fungistatic Itraconazole can antagonize amphotericin B aby reducing its binding target Toxicity: ketoconazole interferes with testosterone and cortisone resulting in gynecomastia and loss of libido hepatitis can be severe(preform liver function test and discontinue if symptoms develop) IV voriconazole can be associated with transient loss of light perception DDI with other drugs that are metabolized by cytochrome p450
46
fluconazole MOA, SE, indication
azole active against candida albicans(can develop resistance with prolonged treatment), Cryptococcus neoformans inactive against: aspergillus, C. glabrata, C. krusei Treatment of choice for oral Candiasis and candida vulvovaginitis
47
treament of choice for systemic fungal infections; oral candiasis
Treatment of choice for oral Candiasis and candida vulvovaginitis is fluconazole systemic fungal infection treatment of choice is amphotericin B
48
itraconazole MOA, SE, indications
azole improved agasint histoplasmosis, coccidiomycosis, blastomycosis, sporotrichosis used in AIDS patient to prevent relapses of histoplasmosis absorption is erratic (unpredictable, capricious, volatile, opaque?[no, that cant be right])
49
what do you use for aspergillus
posaconazole/itraconazole (fluconazole isn't active against it) echinocandins amphotericin B
50
drugs that cause phlebitis
vancomycin | amphotericin B
51
echinocandins name them, their MOA, SE, indications, administration route
block cell wall synthesis by inhibiting synthesis of Bglucan via non competitive inhibition of ,3Beta glucan synthase caspofungin, anidulafungin, micafungin MUST be administered by IV route metabolized by the liver active against aspergillus and candida not active agaisnt cryptococcus ``` indications: intestive aspergilosis (in patients who cant tolerate amphotericin B or itraconazole) ``` toxicity is minimal
52
Flucystosine MOA, SE, Indications
its a flurine analog of cysteine which impairs fungal DNA and RNA synthesis well absorbed orally and cleared by kidneys. penetrates all tissue (including BBB) good agasint C. albicans and cryptococccus neoformes indication cryptococcal meningitis (combination of flucytosine and amphotericin B is faster) toxicity bone marrow suppression (neutropenia, anemia, thrombocytopenia)
53
what favors viral resistance to antiviral drugs
prolonged antiviral therapy and high mutation rate (RNA mutates more than DNA) and high viral load
54
Aciclovir, valaclovir, famciclovir MOA
blocks DNA transcription require viral thymidine kinase phosphorylation for activity acyclovir and valaclovir are synthetic analogs of guanine, acyclovir binds to replicating viral DNA and causes premature termination and inhibits DNA polymerases famciclovir is an acyclic guanosine resistance is mediated by reduction in viral thymidine kinase (all those drugs require thymidine kinase phosphorylation for activity)
55
indications and toxicity for acyclovir/valacyclovir, famciclovir
toxicity is minimal (lethargy, hallucination and seizures) valacyclovir is converted into acyclovir, thus higher levels are achieved when compared to oral preparations of acyclovir indication, excellent against herpes simplex 1 and 2. (herpes encephalitis) toxicity: rash, hematuria, headache, nephrotoxicity , nausea
56
ganciclovir and valganciclovir: MOA, toxicity and usage
gancilovir is a guanine analog that inhibits viral DNA polymerase and requires thymidine kinase for activation. penetrates all tissue vanganciclovir converts into gancilovir used agasint cytomegalovirus, herpes simplex 1,2. varcella and epstein barr virus indications: CMV retinitis, pneumonia, colitis, prophylaxis for the immunocompromised transplant patients toxicity bone marrow suppression CNS confusion, psychosis, coma, seizures
57
cidofovir MOA, usages and toxicity
analog of deoxycytidine monophosphate acts as a competitive inhibitor of viral DNA polymerase causing premature chain termination active against many DNA viruses, CMV, HSV, smallpox, papilloma viruses, adenoviuses indication AMV retinitis in patients with AIDS HSV in patients with AIDS highly nephrotoxic
58
foscarnet, MOA, SE, USAGE
pyrophosphate analog reversibly blocks the pyrophostphate biding site of DNA polymerase indications CMV retinitis and acyclovir resistant mucocutaneous hepres simplex toxicity nephrotoxicity => azotemia, proteinemia
59
interferons MOA
proteins synth by eukaroitc cell in response to viral ifnections upregulates genes with antiviral activity in the host cells indications chronic hepatitis C and b. Kaposi saroma, condiloma acuminatum toxicity influenza like syndrome bone marrow suppression nephrotoxicity
60
what are anti influenza agents and their MOA, indications, toxicity
amantadine and rimantadine bind and inhibit the M2 protein indications: only indiated agaisnt influenza A toxicity CNS effects for Influenza B and A we use Neuraminidaze inhibitors, zanamivir, amantadine, rimantadine, osltamivir bind and inhibit the M2 protein( proton-selective viroporin, integral in the viral envelope ) toxicity is bronchospasm

Infectious disease (6 decks)

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